Pulmonary blood flow distribution during gaseous and partial liquid ventilation (PLV) in experimental acute lung injury (ALI)

2000 ◽  
Vol 17 (Supplement 19) ◽  
pp. 170
Author(s):  
M. Max ◽  
B. Nowak ◽  
R. Dembinski ◽  
R. Kuhlen ◽  
R. Rossaint
Surgery ◽  
1997 ◽  
Vol 122 (2) ◽  
pp. 313-323 ◽  
Author(s):  
Paul G Gauger ◽  
Michael C Overbeck ◽  
Robert A Koeppe ◽  
Barry L Shulkin ◽  
Julia N Hrycko ◽  
...  

2000 ◽  
Vol 93 (6) ◽  
pp. 1437-1445 ◽  
Author(s):  
Martin Max ◽  
Bernd Nowak ◽  
Rolf Dembinski ◽  
Gernot Schulz ◽  
Ralf Kuhlen ◽  
...  

Background It has been proposed that partial liquid ventilation (PLV) causes a compression of the pulmonary vasculature by the dense perfluorocarbons and a subsequent redistribution of pulmonary blood flow from dorsal to better-ventilated middle and ventral lung regions, thereby improving arterial oxygenation in situations of acute lung injury. Methods After induction of acute lung injury by repeated lung lavage with saline, 20 pigs were randomly assigned to partial liquid ventilation with two sequential doses of 15 ml/kg perfluorocarbon (PLV group, n = 10) or to continued gaseous ventilation (GV group, n = 10). Single-photon emission computed tomography was used to study regional pulmonary blood flow. Gas exchange, hemodynamics, and pulmonary blood flow were determined in both groups before and after the induction of acute lung injury and at corresponding time points 1 and 2 h after each instillation of perfluorocarbon in the PLV group. Results During partial liquid ventilation, there were no changes in pulmonary blood flow distribution when compared with values obtained after induction of acute lung injury in the PLV group or to the animals submitted to gaseous ventilation. Arterial oxygenation improved significantly in the PLV group after instillation of the second dose of perfluorocarbon. Conclusions In the surfactant washout animal model of acute lung injury, redistribution of pulmonary blood flow does not seem to be a major factor for the observed increase of arterial oxygen tension during partial liquid ventilation.


1999 ◽  
Vol 91 (6) ◽  
pp. 1861-1861 ◽  
Author(s):  
Steven Deem ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Richard G. Hedges ◽  
Erik R. Swenson

Background Isovolemic anemia results in improved gas exchange in rabbits with normal lungs but in relatively poorer gas exchange in rabbits with whole-lung atelectasis. In the current study, the authors characterized the effects of hemodilution on gas exchange in a distinct model of diffuse lung injury: venous gas embolization. Methods Twelve anesthetized rabbits were mechanically ventilated at a fixed rate and volume. Gas embolization was induced by continuous infusion of nitrogen via an internal jugular venous catheter. Serial hemodilution was performed in six rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; six rabbits were followed as controls over time. Measurements included hemodynamic parameters and blood gases, ventilation-perfusion (V(A)/Q) distribution (multiple inert gas elimination technique), pulmonary blood flow distribution (fluorescent microspheres), and expired nitric oxide (NO; chemoluminescence). Results Venous gas embolization resulted in a decrease in partial pressure of arterial oxygen (PaO2) and an increase in partial pressure of arterial carbon dioxide (PaCO2), with markedly abnormal overall V(A)/Q distribution and a predominance of high V(A)/Q areas. Pulmonary blood flow distribution was markedly left-skewed, with low-flow areas predominating. Hematocrit decreased from 30+/-1% to 11+/-1% (mean +/- SE) with hemodilution. The alveolar-arterial PO2 (A-aPO2) difference decreased from 375+/-61 mmHg at 30% hematocrit to 218+/-12.8 mmHg at 15% hematocrit, but increased again (301+/-33 mmHg) at 11% hematocrit. In contrast, the A-aPO2 difference increased over time in the control group (P < 0.05 between groups over time). Changes in PaO2 in both groups could be explained in large part by variations in intrapulmonary shunt and mixed venous oxygen saturation (SvO2); however, the improvement in gas exchange with hemodilution was not fully explained by significant changes in V(A)/Q or pulmonary blood flow distributions, as quantitated by the coefficient of variation (CV), fractal dimension, and spatial correlation of blood flow. Expired NO increased with with gas embolization but did not change significantly with time or hemodilution. Conclusions Isovolemic hemodilution results in improved oxygen exchange in rabbits with lung injury induced by gas embolization. The mechanism for this improvement is not clear.


1998 ◽  
Vol 84 (5) ◽  
pp. 1540-1550 ◽  
Author(s):  
Allan Doctor ◽  
Juan C. Ibla ◽  
Barry M. Grenier ◽  
David Zurakowski ◽  
Michelle L. Ferretti ◽  
...  

Regional pulmonary blood flow was investigated with radiolabeled microspheres in four supine lambs during the transition from conventional mechanical ventilation (CMV) to partial liquid ventilation (PLV) and with incremental dosing of perfluorocarbon liquid to a cumulative dose of 30 ml/kg. Four lambs supported with CMV served as controls. Formalin-fixed, air-dried lungs were sectioned according to a grid; activity was quantitated with a multichannel scintillation counter, corrected for weight, and normalized to mean flow. During CMV, flow in apical and hilar regions favored dependent lung ( P < 0.001), with no gradient across transverse planes from apex to diaphragm. During PLV the gradient within transverse planes found during CMV reversed, most notably in the hilar region, favoring nondependent lung ( P = 0.03). Also during PLV, flow was profoundly reduced near the diaphragm ( P < 0.001), and across transverse planes from apex to diaphragm a dose-augmented flow gradient developed favoring apical lung ( P < 0.01). We conclude that regional flow patterns during PLV partially reverse those noted during CMV and vary dramatically within the lung from apex to diaphragm.


2002 ◽  
Vol 97 (3) ◽  
pp. 652-659 ◽  
Author(s):  
Christian Putensen ◽  
Jukka Räsänen ◽  
Gabriele Putensen-Himmer ◽  
John B. Downs

Background Rapid recovery and weaning from ventilatory support and cardiovascular stability are suggested advantages of isoflurane inhalation, in concentrations ranging from 0.1 to 0.6 vol%, for long-term sedation in mechanical ventilated patients. This study was designed to determine whether isoflurane in low concentrations impairs pulmonary gas exchange by increasing ventilation and perfusion (V(A)/Q) mismatch during lung injury. Methods Fourteen anesthetized dogs received in random order 0, 0.25, or 0.5 vol% end-tidal isoflurane before and after induction of lung injury with oleic acid. Gas exchange was assessed by blood gas analysis and by estimating the V(A)/Q distributions using the multiple inert gas elimination technique. Results Administration of oleic acid produced a lung injury with severe V(A)/Q mismatch and 38 +/- 4% intrapulmonary shunting of blood. During lung injury, isoflurane accounted for a dose-related increase in blood flow to shunt units from 38 +/- 4 to 42 +/- 3 (0.25 vol%) and 48 +/- 4% (0.5 vol%) (P &lt; 0.05), dispersion pulmonary blood flow distribution from 0.94 +/- 0.07 to 1.01 +/- 0.09 (0.25 vol%) and 1.11 +/- 0.11% (0.5 vol%) (P &lt; 0.05), and a decrease in perfusion of normal V(A)/Q units from 58 +/- 5 to 55 +/- 4 (0.25 vol%) and 50 +/- 4% (0.5 vol%) (P &lt; 0.05) (mean +/- SE). Isoflurane decreased arterial oxygen partial pressure from 72 +/- 4 to 62 +/- 4 mmHg (0.25 vol%) and 56 +/- 4 mmHg (0.5 vol%) (P &lt; 0.05) and oxygen delivery from 573 +/- 21 to 529 +/- 19 ml. kg. min (0.25 vol%) and 505 +/- 22 ml. kg. min (0.5 vol%) (P &lt; 0.05). Gas exchange, perfusion of shunt and normal V(A)/Q units, and pulmonary blood flow distribution was similar in absence of lung injury with and without isoflurane. Isoflurane 0.5 vol% lowered cardiac output during all conditions (P &lt; 0.05). CONCLUSIONS Inhalation of low concentrations of isoflurane contributed to increased V(A)/Q mismatch and decreased systemic blood flow and oxygen delivery in mechanically ventilated animals with injured lungs.


1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.


1999 ◽  
Vol 14 (3) ◽  
pp. 154-160 ◽  
Author(s):  
Masao Tayama ◽  
Nobuaki Hirata ◽  
Tohru Matsushita ◽  
Tetsuya Sano ◽  
Norihide Fukushima ◽  
...  

2000 ◽  
Vol 16 (2) ◽  
pp. 288 ◽  
Author(s):  
T.V. Brogan ◽  
R.G. Hedges ◽  
S. McKinney ◽  
H.T. Robertson ◽  
M.P. Hlastala ◽  
...  

Respiration ◽  
1974 ◽  
Vol 31 (4) ◽  
pp. 289-295
Author(s):  
M. Arborelius, jr. ◽  
V. Lopéz-Majano ◽  
R.C. Reba ◽  
T.K. Natarajan

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